During the early epoch of biological evolution, aluminium was not available for the primitive organisms because of the low solubility of aluminium compounds. This can explain why aluminium is toxic for the present-day living organisms. We studied the toxic effect of aluminium by feeding Drosophila melanogaster adults for 24 hrs. with a 1% sugar solution containing different concentrations of aluminium sulphate. The effect of magnesium chloride was also tested in combination with aluminium. After 24 hrs. we calculated the survival rate, and solubilised the flies in concentrated nitric acid in a microwave oven. The Al, Na, Mg and Zn content of the solubilised flies was measured with the ICP-AES method. We found no change in the Zn content while the Al and Mg content changed according to the treatment, and the Na content decreased significantly (20-30%) in all the cases. We suppose that the flies were mainly killed by the elevated sodium efflux resulting in a decreased intracellular pH. The cause of the elevated Na efflux could be the increased rigidity of the cell membrane caused by the aluminium. We discuss the experimental results and the supposable mechanism of toxicity.
Canthaxanthin (β, β-carotene 4, 4′ dione) is used widely as a drug or as a food and cosmetic colorant, but it may have some undesirable effects on human health, mainly caused by the formation of crystals in the macula lutea membranes of the retina. This condition is called canthaxanthin retinopathy. It has been shown that this type of dysfunction of the eye is strongly connected with damage to the blood vessels around the place of crystal deposition. This paper is a review of the experimental data supporting the hypothesis that the interactions of canthaxanthin with the lipid membranes and the aggregation of this pigment may be the factors enhancing canthaxanthin toxicity towards the macula vascular system. All the results of the experiments that have been done on model systems such as monolayers of pure canthaxanthin and mixtures of canthaxanthin and lipids, oriented bilayers or liposomes indicate a very strong effect of canthaxanthin on the physical properties of lipid membranes, which may explain its toxic action, which leads to the further development of canthaxanthin retinopathy.
The present study was designed to evaluate the effects of nonylphenol in the pro-oxidant/ antioxidant system in ovary of the cichlid fish Etroplus maculatus. Fishes were exposed at two sublethal concentrations (one-fifth and one-tenth of LC50) of nonylphenol for 24, 72 and 96 h maintaining control groups. The oxidative stress indices as the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase along with the levels of hydrogen peroxide generation and lipid peroxidation were monitored in concentration- and time-dependent manner. Activity of superoxide dismutase significantly (P<0.05) increased at both concentrations in timedependent manner. Meanwhile the activities of catalase and glutathione reductase significantly (P<0.05) decreased after 72 and 96 h of nonylphenol treatment. The levels of hydrogen peroxide generation and lipid peroxidation increased in all treatment groups when compared to controls. The present results demonstrated that the induction of oxidative stress in ovary of fish by the generation of lipid peroxidation could be due to the exposure of environmental contaminant, nonylphenol. Therefore, the observed oxidative stress in ovary can be indicated as a mechanism of toxicity in the fish exposed to nonylphenol.
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